Reperfusion of cerebral vessels following total cerebral ischemia of more than five minutes has been shown to be impaired and this is possibly the initial irreversible factor causing neurological sequella. Chiang et al, have shown that ischemic perivascualr glial and endothelial cell swelling possibly causes this phenomenon in rabbits. Post ischemic structural changes in vessels and perivascular glia have not been found in rats and monkeys. In preliminary work in rabbits, we have shown that the amount of impairment of cerebral reperfusion is inversely related to the pressure of the post ischemic infusion. Acute hemodilution with saline in acute experiments greatly improved cerebral reperfusion following fifteen minutes of ischemia. This latter finding suggests that rheological factors may play a very important role. Our objective is to determine by electron and light microscopy whether ischemia causes the vascular swelling described when sludging is minimized, thus maximizing fixative infusion and tissue fixation. In rabbits total cerebral ischemia will be produced by aortic cross clamping. Saline will be infused through an intraaortic cannula during the first three minutes of aortic occlusion to replace all of the blood in the cerebral vessels. Fifteen minutes of aortic clamping (five minutes of clamping in controls will be terminated by the infusion of glutaraldehyde and formaldehyde (method of Peters) at sufficiently high pressure to assure complete perfusion of all vessels. After dehydrating and embedding the tissue specimens in epoxy, the brain capillaries and perivascular glia will be studied using an electron microscope. Conventional paraffin sections will also be examined. Our second objective is to determine whether acute hemodilution will achieve increased rate and quality of survival of rabbits subjected to transient total cerebran ischemia by basilar artery and bilateral common carotid artery clipping (method of Kowada et al).